Cause Of Venous Thrombosis Research Articles

S2746 Mesenteric Venous and Portal Vein Thrombosis in a Patient With Ulcerative Colitis: Delayed Post-Operative Presentation or Hypercoagulable State?

Introduction: Mesenteric venous thrombosis (MVT) and portal vein thrombosis (PVT) are conditions involving occlusion of the vascular supply of the intestinal system. The symptoms of MVT and PVT may be nonspecific, however, patients may present with acute abdominal pain. The cause of venous thrombosis of the gastrointestinal system may be multifactorial, including patients with pro-coagulable conditions. Here we present the case of a patient with ulcerative colitis (UC) who underwent a recent colectomy with end ileostomy and arrived at the Emergency Department (ED) with acute abdominal pain secondary to superior mesenteric vein thrombosis extending into the portal vein. Case Description/Methods: This is the case of a 40-year-old male with a history of refractory ulcerative colitis diagnosed 7 years before admission, with evidence of disease on descending, sigmoid, and rectum. He underwent laparoscopic total abdominal colectomy with end ileostomy a month before admission. His symptoms were controlled with Ustekinumab and Prednisone tapering. The patient arrives at the ED with symptoms of tenesmus, generalized abdominal pain, and rectal bleeding. His physical examination was remarkable for hemodynamic stability and diffuse abdominal pain on palpation, without rebound or guarding. Abdominopelvic computed tomography with intravenous contrast revealed a large intramural thrombus extending from the superior mesenteric vein into the portal vein. The patient was started on an intravenous heparin drip, which was transitioned to direct oral anticoagulation therapy prior to discharge. Discussion: Patients with ulcerative colitis who require surgical intervention are at an increased risk of thromboembolic events. Here, we presented the case of a patient with evidence of extensive portomesenteric thrombosis with delayed onset after surgical intervention. Post-operative thrombosis is prevalent within 7-10 days after surgery. However, our patient presented with extensive thrombosis more than 1 month after the intervention. Our case raises concerns regarding the multifactorial etiology of the patient’s presentation. Moreover, UC has been known to increase prothrombotic state. Therefore, this case highlights how MVT in patients with UC may be secondary to a combination of factors, such as the hypercoagulable state of UC due to chronic inflammation and mechanical endothelial injury from surgical intervention. Prompt evaluation is essential to prevent intestinal infarction and reduce morbidity and mortality in these patients.

Uterine fibroids and the problem of deep vein thrombosis of the lower extremities. View of a vascular specialist and hematologist

The article provides clinical data and an algorithm for the management of patients with symptomatic uterine fibroids complicated by metrorrhagia and venous thrombotic events.Objective: to improve the treatment of patients with uterine fibroids complicated by abnormal menstrual bleeding, anemia and venous thrombotic events due to the implementation of the developed algorithm for diagnosis and treatment.Materials and methods. The study included 15 patients aged 32–49 years with a diagnosis of uterine fibroids with menorrhagia and iron deficiency anemia, complicated by deep vein thrombosis of the lower extremities. Thromboembolism of small branches of the pulmonary artery was diagnosed in 5 (30%) of these patients.The examination algorithm included general clinical tests (general blood and urine analysis, biochemical blood analysis, coagulogram), evaluation of the D-dimer, soluble fibrin monomer complexes, ultrasound of the pelvic organs, ultrasound duplex scanning of the veins of lower extremities, electrocardiography, echocardiography, multispiral computed tomography of chest. All patients underwent endometrial biopsy to exclude oncological pathology.The proposed treatment included: uterine artery embolization to stop bleeding, correction of hemostatic parameters, and anticoagulant therapy of venous thrombotic events after stopping bleeding.Results. Bleeding was stopped in all 100% of patients after endovascular uterine artery embolization. The duration of anticoagulant therapy depended on the causes of venous thrombosis and was at least 3–6 months; it was extended for more than 6 months if there were concomitant risk factors.Conclusions. Uterine artery embolization allows quickly and reliably stopping bleeding and immediately starting adequate anticoagulant therapy for venous thrombotic events.

IL-17B Regulates Endothelial Cell Apoptosis in Venous Thrombosis

Venous thromboembolism (VTE) is the comorbidity of deep vein thrombosis (DVT) and pulmonary embolism (PE); it is an urgent public health problem. The primary cause of venous thrombosis is endothelial dysfunction caused by vascular injury and inflammation or overexpressed procoagulant factors. Previous studies have shown that vascular endothelial cell apoptosis is involved in venous thrombosis, causing vascular wall damage. The pro-inflammatory cytokine interleukin-17 (Il-17A) induces endothelial cell apoptosis and promotes thrombosis. However, it remains unclear whether other IL-17 family cytokines are involved in thrombus formation. Among the IL-17 family, IL-17B is less well-characterized. Several studies have reported that IL-17B could stimulate TNF-α, IL-1, and IL-6 expression in macrophages. Furthermore, IL-17B induced activation of the ERK1/2 pathway, upregulating Bcl-2 family anti-apoptotic proteins in breast tumors. However, it is unclear whether IL-17B is involved in thrombus formation by regulating endothelial apoptosis. Therefore, this study aimed to examine whether IL-17B could affect endothelial apoptosis by promoting thrombus formation.

Elevated miR-195-5p expression in deep vein thrombosis and mechanism of action in the regulation of vascular endothelial cell physiology.

Deep vein thrombosis (DVT) is one of the most common cardiovascular diseases. The apoptosis of vascular endothelial cells is the most important cause of venous thrombosis. MicroRNAs (miRNAs) play important roles in the regulation of cell apoptosis. miRNA (miR)-195 is upregulated in the blood of patients with DVT, and it was predicted that Bcl-2 is a potential target of miR-195-5p. Therefore, it was hypothesized that miR-195-5p may play an important role in the development of DVT by targeting Bcl-2. The present study aimed to investigate the expression of miR-195-5p in DVT patients, and to explore whether miR-195-5p is involved in the development of DVT by regulating the apoptosis of vascular endothelial cells. The level of miR-195-5p was detected using reverse transcription-quantitative PCR. Dual luciferase reporter assays were used to determine the relationship between Bcl-2 and miR-195-5p. Cell viability was detected using MTT assays, and cell apoptosis was analyzed by flow cytometry. Protein levels of Bcl-2 and Bax were measured by western blotting. The results indicated that miR-195-5p was significantly upregulated in the blood of DVT patients. It was also revealed that Bcl-2 was a direct target of miR-195-5p, and that Bcl-2 was downregulated in the blood of patients with DVT. miR-195-5p downregulation promoted cell viability and inhibited the apoptosis of human umbilical vein endothelial cells (HUVECs). miR-195-5p upregulation inhibited cell viability and increased the apoptosis of HUVECs. All of the observed effects of miR-195-5p upregulation on HUVECs were reversed by raised Bcl-2 expression. In conclusion, miR-195-5p was significantly upregulated in patients with DVT, and it may be involved in the development of DVT by regulating the apoptosis of vascular endothelial cells. Therefore, miR-195-5p may be a potential target for predicting and treating DVT.

Blood coagulation in venous thrombosis, complicating treatment of children, adolescents and young adults with lymphomas

Objective of the study was to compare blood clotting parameters in lymphoma patients with or without venous thrombosis (VT), as well as to analyze the duration and outcome of anticoagulant therapy in children, adolescents and young adults with lymphoma, whose program treatment was complicated by VT.Materials and methods . The analysis included 28 patients with lymphoma (Hodgkin lymphoma – 5, non-Hodgkin lymphoma – 23), aged from 2 to 25 years (median – 16.0 years), whose program treatment in 2005–2017 was complicated by VT. The case-control study was carried out to compare the parameters of blood coagulation. The control group consisted of 22 patients, aged from 2 to 20 years (median – 15.5 years) with the same diagnosis, age, therapy protocol and phase of treatment who had no thrombotic complications. The comparison group consisted of 35 healthy children aged from 3 to 18 years (median – 14.0 years).Results . There was no difference in majority of blood clotting parameters in lymphoma patients with or without VT. Hyperfibrinogenemia and an increased D-dimers level distinguished patients with lymphoma, regardless of the presence or absence of thrombosis, from healthy children of the same age (р<0.05). Anticoagulant therapy up to 3 months received 10 patients, for 4–6 months – 4, for 7–12 months – 12, up to 18 months – 2. One adult patient with a homozygous mutation 20210G>A gene of the factor II takes warfarin continuously for a long time after relapse of VT. Complete recanalization of the thrombosed vessel occurred within the first 3 months in 9 patients, within 4–6 months – in 1, within 7–12 months ‒ in 4. Partial recanalization within 3–12 months was confirmed in 8 patients. Vein obliteration, mainly the internal jugular vein, as the outcome of VT occurred in 6 patients within 4–12 months.Conclusion . Detection of routine blood clotting parameters does not allow identifying patients with thrombosis among children, adolescents and young adults with lymphoma. Fibrinogen and D-dimers levels were significantly higher in lymphoma patients, than in healthy children. Anticoagulant therapy for 3–12 months led to the complete or partial recanalization of VT in 79 % of patients. To detect blood clotting parameters by thrombosis development, as well as to reveal and monitor transient and permanent risk factors are necessary to specify the cause of VT and to determine the appropriate anticoagulant therapy.

The cause analysis and nursing care of patients with venous thrombosis induced by PICC

Objective To explore the causes of venous thrombosis after peripherally inserted central catheter(PICC) in tumor patients and corresponding nursing precautions. Methods A total of 105 patients with tumors undergoing long-term infusion and chemotherapy in this hospital were selected as the research subjects.All patients were treated with PICC catheterization.Nursing measures were observed and administered at the beginning of catheterization. Results A total of 6 patients developed venous thrombosis, and the patients' condition gradually recovered after anticoagulation therapy.It was found that venous thrombosis was not only directly related to catheterization, but also related to drug use in the course of disease treatment and activity of patients. Conclusion Skilled puncture techniques and related nursing measures can effectively reduce the occurrence of venous thrombosis in patients with PICC. Key words: Venous thrombosis; PICC; Nursing measures

Identification of mutations in SLC4A1, GP1BA and HFE in a family with venous thrombosis of unknown cause by next-generation sequencing.

Various risk factors, including high age, female gender, obesity and certain genetic defects have been linked to venous thrombosis. A Taiwanese family with venous thrombosis of unknown cause were enrolled in the present study. In this pedigree, two women without any specific underlying diseases suffered from venous thrombotic events at the same age. No specific risk factors or coagulation abnormalities were identified. The main proband's younger brother also had intestinal arterial thrombosis at 54 years of age. Therefore, it was hypothesized that familial genetic defects may be the cause of venous thrombosis within this family. Blood samples collected from certain members of this pedigree were subjected to whole-exome sequencing, and three genetic variants were identified, including a missense variant of solute carrier family 4 member 1 (SLC4A1) (c.388G>A), a deletion on glycoprotein Ib platelet α subunit (GP1BA) (c.1322_1344del23) and an insertion in the splice site of homeostatic iron regulator (HFE). To date, none of these three genetic variants have been reported to be associated with venous thrombosis, to the best of our knowledge. The present study suggests that these genetic variants of SLC4A1, GP1BA and HFE may be associated with venous thrombosis in an Asian pedigree.

Left Common Femoral Vein Thrombosis with Lower Limb Gangrene in A Newborn

Gangrene in the newborn following deep vein thrombosis is extremely rare and may be congenital and acquired. We report an eleven day term male baby presented in emergency with bluish colouration of left lower limb for two days, which progressed to gangrene on fourth day of admission. The baby was initially treated with low molecular weight heparin followed by warfarin and antimicrobials (cefotaxime and piperacillin). Knee disarticulation was done on the fourth day of admission. On postoperative days, baby was well, and discharged on warfarin therapy. The exact cause for venous thrombosis could not be established. This case is reported because of possible idiopathic gangrene in the newborn with highlights of management.

Renal vein to renal collecting system fistula: An extreme complication from central venous thrombosis secondary to indwelling catheter

Abstract Central venous catheters are routinely used for resuscitation, chemotherapy and nutrition but are not without risk. Central lines are the most common extrinsic cause of venous thrombosis in neonates and infants. We present an ex-36 week 1800g infant baby girl recovering after a staged repair of gastroschisis with ileostomy and mucous fistula formation. The patient was receiving parenteral nutrition through an indwelling saphenous vein tunneled catheter, with its tip in the inferior vena cava. The patient developed polyuria, with a characteristic odor of the parenteral nutrition and a urine analysis showed glucose and triglyceride levels consistent with the composition of the parenteral nutrition fluid. A fluoroscopic cysto-urogram and an inferior vena-cavogram showed a catheter-associated inferior vena cava thrombosis leading to backpressure changes, diverting all intravenous contrast into the right renal vein and to renal collecting system, thus elucidating the route of the parenteral nutrition fluid reaching the bladder. Our case represents an extreme case of complicated central venous thrombosis. We emphasize the importance of practicing a high index of suspicion for thrombotic complications in severely ill neonates with central venous access. An early diagnosis and aggressive management may prevent progression of the disease towards an overwhelming complication.

Non-Catheter-related Venous Thromboembolism in Children: Imaging Review from Head to Toe.

Non-catheter-related venous thromboembolism (VTE) is less common in children than in adults. Although the presence of a central venous catheter is the most common cause of venous thrombosis in children, infection and inflammation, malignancy, hypercoagulability, dehydration, and certain sites of normal variant and pathologic anatomic narrowing all predispose to VTE in children. The mortality and morbidity of VTE vary according to the underlying cause, including whether malignancy is present. Various modalities including ultrasonography (US), computed tomography, and magnetic resonance imaging can be used to image VTE, with some modalities better suited to particular parts of the body and clinical scenarios than others. When feasible, US is the initial test of choice for the diagnosis of VTE. US findings of acute VTE include a dilated noncompressible vein, intraluminal echoes, lack of color flow, and abnormal spectral venous waveforms. Serial US examinations are useful for monitoring patient response to therapy; a normal compressible vein will be seen after complete resolution of thrombus, and chronic venous changes including wall thickening, intraluminal webs, and phleboliths, which are readily apparent at US. Accurate and timely diagnosis of VTE must take into account the various advantages and disadvantages of each modality including speed, accuracy, availability, exposure to ionizing radiation, and need for sedation, as well as the clinical stability and transportability of the child. This article reviews some of the more common causes of VTE in children (other than those related to a central venous catheter) according to body part and discusses the associated imaging findings. ©RSNA, 2017.

Thrombophilia And Arterial Ischemic Stroke

Ischemic stroke (IS) is a common cause of morbidity and mortality with significant socioeconomic impact especially when it affects young patients. Compared to the older adults, the incidence, risk factors, and etiology are distinctly different in younger IS. Hypercoagulable states are relatively more commonly detected in younger IS patients.Thrombophilic states are disorders of hemostatic mechanisms that result in a predisposition to thrombosis .Thrombophilia is an established cause of venous thrombosis. Therefore, it is tempting to assume that these disorders might have a similar relationship with arterial thrombosis. Despite this fact that 1-4 % of ischemic strokes are attributed to Thrombophillia, this alone rarely causes arterial occlusions .Even in individuals with a positive thrombophilia screen and arterial thrombosis, the former might not be the primary etiological factor.Thrombophilic disorders can be broadly divided into inherited or acquired conditions. Inherited thrombophilic states include deficiencies of natural anticoagulants such as protein C, protein S, and antithrombin III (AT III) deficiency, polymorphisms causing resistance to activated protein C(Factor V Leiden mutation), and disturbance in the clotting balance (prothrombin gene 20210G/A variant). Of all the inherited thrombophilic disorders, Factor V Leiden mutation is perhaps the commonest cause. On the contrary, acquired thrombophilic disorders are more common and include conditions such as the antiphospholipid syndrome, associated with lupus anticoagulant and anticardiolipin antibodies.The more useful and practical approach of ordering various diagnostic tests for the uncommon thrombophilic states tests should be determined by a detailed clinical history, physical examination, imaging studies and evaluating whether an underlying hypercoagulable state appears more likely.The laboratory thrombophilia screening should be comprehensive and avoid missing the coexisting defect and It is important that a diagnostic search protocol includes tests for both inherited and acquired thrombophilic disorders.Since the therapeutic approach (anticoagulation and thrombolytic therapy) determines the clinical outcomes, early diagnosis of the thrombophilic disorders plays an important role. Furthermore, the timing of test performance of some of the thrombophilic defects (like protein C, protein S, antithrombin III and fibrinogen levels) is often critical since these proteins can behave as acute phase reactants and erroneously elevated levels of these factors may be observed in patients with acute thrombotic events. On the other hand, the plasma levels of vitamin K-dependent proteins (protein C, protein S and APC resistance) may not be reliable in patients taking vitamin K antagonists. Therefore, it is suggested that plasma-based assays for these disorders should be repeated3 to 6 months after the initial thrombotic episode to avoid false-positive results and avoid unnecessary prolonged anticoagulation therapy. The assays for these disorders are recommended after discontinuation of oral anticoagulant treatment or heparin for at least 2 weeks.

The Role of Factor V Leiden 1691G>A and Prothrombin Gene 20210G>A Mutations in Hypercoagulable State Associated with Venous Thromboembolism among Sudanese Patients

Background: Factor V Leiden (FVL) 1691G>A and Prothrombin (PRT) 20210G>A mutations are the most frequent hereditary cause of venous thrombosis in Caucasian and less frequency in African. The aim of this study was to detect the frequency of FVL 1691G>A and PRT 20210G>A mutations among Sudanese venous thromboembolism (VTE) patients. Material and Methods: This was descriptive Cross sectional study in which a total of 176 Sudanese subjects were enrolled in the period between July 2015 and July 2016. Among them, 38 apparently healthy Sudanese individuals as controls and 138 patients (47 males and 91 females), age range 18-90 with documented VTE confirmed by Duplex Doppler ultrasound at Khartoum Teaching Hospital and Sudan Heart Institute were included. Result: In this study, the mean age was 48 years and 67% of total VTE patients were over the age of 40 years. Increased age was noted in the VTE patients with over 34% over the age of 60 years. The controlled subjects included significantly younger individual with 92.1% under the age of 50 and 81.5% under the age of 40 years. The FVL 1691G>A and PRT 20210G>A mutations were totally absent among the studied population. Conclusion: The FVL 1619G>A and PRT 20210G>A mutations were totally absent among Sudanese VTE patients.

Sudden Thrombosis in Coronary Artery Bypass Grafting Surgery

Sudden Thrombosis in Coronary Artery Bypass Grafting Surgery

Uterine myoma as a cause of iliac vein thrombosis and pulmonary embolism: common disease, rare complication.

Uterine myoma is a common condition among women, which may very rarely be associated with deep venous thrombosis (VT). Few reports of myoma with associated VT have been reported in the English language and, of those, only three were associated with embolic events. This manuscript reports the case of a 29-year-old patient who presented with pulmonary embolism due to iliac VT secondary to extrinsic compression by a uterine myoma. Considering the high prevalence of myoma in the population, it is advisable to specifically consider this hypothesis in the case of female patients with pulmonary embolism or limb VT and menstrual abnormalities. This will help to avoid extensive thrombophilia investigation and to accurately determine the correct cause of VT.

Lower Plasma Creatinine and Urine Albumin in Individuals at Increased Risk of Type 2 Diabetes with Factor V Leiden Mutation

The factor V Leiden (FVL) mutation is the most frequent genetic cause of venous thrombosis in Caucasians. However, protective effects have been suggested to balance the disadvantages. We have recently observed protective effects of FVL mutation on experimental diabetic nephropathy in mice as well as an association with reduced albuminuria in two human cohorts of diabetic patients. In the present study we aimed to reevaluate these findings in an independent, larger cohort of 1905 Caucasians at risk of developing type 2 diabetes and extend possible associations to earlier disease stages of nephropathy. Carriers of FVL mutation had a significantly lower urine albumin excretion (P = 0.03) and tended to have lower plasma creatinine concentrations (P = 0.07). The difference in plasma creatinine concentrations was significant after adjustment for the influencing factors: age, gender, and lean body mass (P = 0.048). These observations at a very early “disease” stage are an important extension of previous findings and suggest that modification of glomerular dysfunction by FVL mutation is relevant during very early stages of diabetic nephropathy. This makes the underlying mechanism an interesting therapeutic target and raises the question whether FVL mutation may also exert protective effects in other glomerulopathies.

Occult antithrombin deficiency manifesting as extensive superficial venous thrombosis after venous cannulation

Occult antithrombin deficiency manifesting as extensive superficial venous thrombosis after venous cannulation

Estados hipercoagulables primario y deficiencia de proteínas "C" y "S". Reporte de un caso y revisión de la literatura.

We present a patient with upper gastrointestinal bleeding and gastric varices due to mesenteric and splenic thrombosis related with a hypercoagulable state secondary to protein C and proteins S deficiency. We also did a review of the literature about deficiency of these proteins and their importance as a cause of venous thrombosis not well recognize yet. KEY WORDS: Protein C, Protein S, hypercoagulable state, venous thrombosis, upper gastrointestinal bleeding.

PROC c.574_576del polymorphism: a common genetic risk factor for venous thrombosis in the Chinese population

There are ethnic differences in the genetic risk factors for venous thrombosis (VT). The genetic causes of VT in the Chinese population are not fully understood. To identify possible common abnormal factors that could contribute to thrombosis susceptibility. We measured the levels of nine types of plasma coagulation factor, three types of anticoagulation factor and two types of fibrinolytic factor in 310 VT patients. Factor V activity was higher in 32 cases. Eleven of the 32 cases also had low protein C (PC) or protein S (PS) activities, indicating PC or PS deficiency. No other abnormalities were observed in the other 21 cases. All of the samples were sensitive to activated PC inactivation. Therefore, the abnormal factor involved may be FV inactivator or its cofactor rather than FV itself. Resequencing identified a common PROC c.574_576del variant in 10 of the 32 subjects. In a case-control study, this variant was detected in 68 of the 1003 patients and in 25 of the 1031 controls. It had an adjusted odds ratio of 2.71 (95% confidence interval [CI] 1.68-4.36). PC amidolytic activities of most variant carriers were similar to those of non-carriers, but the mean anticoagulant activity was only 72.7 U dL(-1). Expression studies in vitro showed that the anticoagulant activity of the mutant PC was 43.6% of that of the wild-type PC. We identified what is, so far, the most common genetic risk factor for VT in the Chinese population, with its prevalence being approximately 2.36%.

Traitements spécifiques au milieu psychiatrique et thrombogenèse

The causes of venous thrombosis (DVT) are multifactorial. Psychiatric patients present several etiologic features. Our objective was to determine the role of specific treatments of the psychiatric community on thrombogenesis. retrospective, descriptive and analytical study of 20 cases of DVT in psychiatric patients. We searched MEDLINE (PubMed) between 1959 and 2009. We reviewed article titles and abstracts and full text of selected studies of psychiatric patients with venous thromboembolism (VTE) disease. We identified 31 studies that investigated the association between psychiatric disease and venous thromboembolic events. Our population was young, with an average age of 44.8 years. Lower limb VT is predominant (16 cases). The most common psychiatric disorders are: anxiety-depression (12 cases), unclassifiable psychotic disorders (seven cases) and major depressive disorder (five cases). Their average duration was of 6.4 years. Seventy percent of our patients were taking first generation neuroleptics (NLP), of short half-life (13/14 cases) and at high doses (11/14 patients). Our sample is characterized by the frequency of thrombophilia (45%) and detention in a psychiatric community (35%). Our results are relatively consistent with aggregate data from the literature, underlining a facilitating and pejorative role of the psychiatric community with regard to venous thromboembolic disease. In the psychiatric community, venous thromboembolic disease is conditioned by a combination of several thromboembolism risk factors: linked in part to the psychiatric illness itself; but above all to the specific therapeutic methods in the psychiatric community (antipsychotics, restraint…) which are easily preventable. The relationship between antipsychotic medication and VTE was first suggested about four decades ago, only a few years after the introduction of phenothiazines and reserpine. An association between atypical antipsychotic agents and VTE has been previously suggested for clozapine among young adults with psychiatric disorders. More recently, an increased risk of VTE was suspected for olanzapine or risperidone. The risk for VTE seems to be highest during the initial months of treatment with antipsychotics. Several biological mechanisms of action have been proposed to explain this relationship. One plausible mechanism derives from research suggesting that conventional antipsychotic drugs are associated with enhanced platelet aggregation. A second possible explanation stems from the presence of anticardiolipin antibodies, which increase the risk of venous or arterial thrombosis, as well as in some patients prescribed chloropromazine. A third hypothesis is that venous stasis exacerbated by sedation, commonly found in patients treated with low-potency antipsychotic drugs, may contribute to processes that increase the risk of thrombosis. Other than the medical aspect, the psychiatric community itself is characterized by a large number of variables, providing a particularly encouraging and derogatory hypothesis on the advent and development of VTE.

Lower extremity venous thrombosis in patients younger than 50 years of age

AimLower extremity deep venous thrombosis in the young adult is uncommon and has not been well studied in the literature. The aim of this study is to define risk factors for deep venous thrombosis among patients younger than 50 years of age, to compare them with a control group, and to suggest recommendations for the management and treatment of venous thrombosis in this particular group of patients.MethodsFrom January 2003 to January 2011, 66 consecutive Lebanese patients (29 males and 37 females) younger than 50 years, diagnosed in an academic tertiary-care center with lower extremity deep venous thrombosis by color flow duplex scan, were retrospectively reviewed. Their age varied between 21 and 50 years (mean 38.7 years). The control group included 217 patients (86 males and 131 females) older than 50 years (range: 50–96 years; mean 72.9 years).ResultsThe most commonly reported risk factors in the younger age group were inherited thrombophilia (46.9% compared with 13.8% in the control group; P < 0.001), pregnancy (18.2% compared with 0.5%; P < 0.001), treatment with estrogen drugs (13.6% compared with 2.3%; P = 0.001), and family history of venous thromboembolism (9.1% compared with 3.8%; P = 0.084).ConclusionInherited thrombophilia is the most commonly observed risk factor among patients younger than 50 years, with a prevalence of three times more than the control group. Young adults should be screened for thrombophilia even in the presence of transient acquired risk factors. Pregnancy and treatment with estrogen drugs essentially when associated with inherited thrombophilia represent a frequent cause of venous thrombosis among young female patients. Inferior vena cava abnormalities should be excluded in young patients with spontaneous proximal venous thrombosis especially when recurrent venous thrombosis or resistance to anticoagulation are observed.